With New Ebola Model, UW Scientists Track Genetics of Host Resistance

November 19th 2014

Angela Rasmussen, Research Assistant professor at the University of Washington

Scientists around the world are racing to learn more about the ongoing Ebola virus outbreak in West Africa, which as of November 2014 had claimed nearly 5,000 lives and infected more than 13,000. Thanks to remarkable new work from researchers at the University of Washington and collaborators at the University of North Carolina and Rocky Mountain Laboratories, there’s a new tool in the battle against this virus: a collection of lab mice that closely model the types and progression of Ebola seen in humans.

Until now, scientists seeking to understand virus biology or screening drug compounds, among other activities, were limited in their ability to use model organisms. The mouse model for Ebola did not display similar phenotypes to humans infected with the virus. Conducting research on the non-human primate that best models human responses to Ebola — the rhesus macaque — is expensive, challenging, and ethically complicated, says Angela Rasmussen, a research assistant professor in the microbiology department at the University of Washington and lead author on this new project.

Rasmussen and her colleagues aimed to design a better model, and they started with a community resource that has successfully delivered improved mouse models for other research areas: the Collaborative Cross program, which is currently managed at the University of North Carolina. She also pulled in another tool that has worked well for her in the past: Ingenuity Pathway Analysis (IPA) from QIAGEN Bioinformatics, which she deploys to analyze complex transcriptomic data. Between these tools, Rasmussen not only developed an important new model for Ebola research, but she also discovered significant details about effects of host genetics on infection outcomes.

The new mice, featured in the paper just published in Science, display all three major phenotypes seen among humans infected with Ebola: hemorrhagic fever, death, and resistance to lethal infection. “We can now use mice to really model the full breadth of Ebola outcomes that we see in human populations — for example, in the current outbreak,” Rasmussen says. Her team’s findings are reported in a paper entitled “Host genetic diversity enables Ebola hemorrhagic fever pathogenesis and resistance.”